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Archive - Jun 22, 2013


Synchrotron Reveals Odd Bedfellows in 250-Million-Year-Old Fossilized Burrow

Synchrotron imaging has revealed an ancient odd couple - 250 million years ago, a mammal forerunner and an amphibian shared a burrow (synchroton image at left shows contents of fossilized burrow). Scientists from South Africa, Australia, and France have discovered a world-first association while scanning a 250-million-year-old fossilized burrow from the Karoo Basin of South Africa. The burrow revealed two unrelated vertebrate animals nestled together and fossilized after being trapped by a flash flood event. Facing harsh climatic conditions subsequent to the Permo-Triassic (P-T) mass extinction, the amphibian Broomistega and the mammal forerunner Thrinaxodon cohabited in a burrow. Scanning shows that the amphibian, which was suffering from broken ribs, crawled into a sleeping mammal's shelter for protection. This research suggests that short periods of dormancy, called aestivation, in addition to burrowing behavior, may have been a crucial adaptation that allowed mammal ancestors to survive the P-T extinction. The results of this research were published online in an open-access article in PLoS ONE on June 21, 2013. The international team of scientists was led by Dr. Vincent Fernandez from Wits University, South Africa and the European Synchrotron Radiation Facility (ESRF) in Grenoble, France. The other authors from Wits University included Professor Bruce Rubidge (Director of the newly formed Palaeosciences Centre of Excellence at Wits), Dr. Fernando Abdala, and Dr. Kristian Carlson. Other authors include Dr. Della Collins Cook (Indiana University); Dr. Adam Yates (Museum of Central Australia), and Dr. Paul Tafforeau (ESRF).

Green Algae Need Hemoglobin to Survive in an Oxygen-Free Environment

When green algae "can't breathe," they get rid of excess energy through the production of hydrogen. Biologists at the Ruhr-Universität Bochum in Germany have found out how the cells notice the absence of oxygen. For this, they need the messenger molecule nitric oxide and the protein hemoglobin, which is commonly known from red blood cells of humans. With colleagues at the UCLA, the Bochum team reported its results online on June 10, 2013 in PNAS. In the human body, hemoglobin transports oxygen from the lungs to the organs and brings carbon dioxide, which is produced there, back to the lungs. "However, scientists have known for years that there is not just the one hemoglobin," says Professor Thomas Happe from the Work Group Photobiotechnology. Nature has produced a large number of related proteins which fulfill different functions. The green alga Chlamydomonas reinhardtii has what is known as a "truncated" hemoglobin, the function of which was previously unknown. Dr. Happe's team has deciphered its role in surviving in an oxygen-free environment. When Chlamydomonas has no oxygen available, the algae transfer excess electrons to protons, creating hydrogen (H2). "For this to work, the green alga activates a certain gene program and creates many new proteins," Dr. Happe explains. "But how exactly the cells even notice that oxygen is missing is something we did not know." The research team looked for genes that are particularly active when green algae have to live without oxygen – and found a gene that forms the blueprint for a hemoglobin. In an oxygen-rich environment, however, this gene was completely idle. The scientists studied the hemoglobin protein and its genetic blueprint in more detail using molecular biological and biochemical analyses. "One thing became clear very quickly," says Dr.

Alzheimer's-Disease-Associated Protein Controls Movement in Mice

Researchers in Berlin and Munich, Germany and Oxford, United Kingdom, have revealed that a protein well known for its role in Alzheimer's disease controls spindle development in muscle and leads to impaired movement in mice when the protein is absent or treated with inhibitors. The results, which were published online on June 21, 2013 in an open-access article in The EMBO Journal, suggest that drugs under development to target the beta-secretase-1 protein, which may be potential treatments for Alzheimer's disease, might produce unwanted side effects related to defective movement. Alzheimer's disease is the most common form of dementia found in older adults. The World Health Organization estimates that approximately 18 million people worldwide have Alzheimer's disease. The number of people affected by the disease may increase to 34 million by 2025. Scientists know that the protein beta-secretase-1 or Bace1, a protease enzyme that breaks down proteins into smaller molecules, is involved in Alzheimer's disease. Bace1 cleaves the amyloid precursor protein and generates the damaging Abeta peptides that accumulate as plaques in the brain leading to disease. Now scientists have revealed in more detail how Bace1 works. "Our results show that mice that lack Bace1 proteins or are treated with inhibitors of the enzyme have difficulties in coordination and walking and also show reduced muscle strength," remarked Dr. Carmen Birchmeier, one of the authors of the paper, Professor at the Max-Delbrück-Center for Molecular Medicine in Berlin, Germany, and an EMBO Member. "In addition, we were able to show that the combined activities of Bace1 and another protein, neuregulin-1 or Nrg1, are needed to sustain the muscle spindles in mice and to maintain motor coordination." Muscle spindles are sensory organs that are found throughout the muscles of vertebrates.

Targeting Antioxidant Enzymes May Kill Metastasizing Cancer Cells

A new study by a team of researchers from the University of Notre Dame provides an important new insight into how cancer cells are able to avoid the cell death process. The findings may suggest a chemotherapeutic approach to prevent the spread of cancers. Metastasis, the spread of cancer from one organ to other parts of the body, relies on cancer cells’ ability to evade a cell death process called anoikis, according to Dr. Zachary T. Schafer, Coleman Assistant Professor of Cancer Biology at Notre Dame. Metastasizing cancer cells are able to survive anoikis, which normally results from detachment from the extracellular matrix. However, Schafer notes that the molecular mechanisms cancer cells detached from the extracellular matrix use to survive has not been well understood. "This paper reveals that cancer cells that are detached from their normal environment, as they would be during metastasis, rely on the activity of antioxidant enzymes to facilitate their survival," Dr. Schafer said. "This class of enzymes is critical for neutralizing oxidative stress and function much like the compounds that are present in a variety of foods." The paper describes a prominent role for antioxidant enzymes in facilitating the survival of breast cancer cells after detachment from the extracellular matrix. Conversely, the researchers report, silencing antioxidant enzyme expression reduced tumor formation. "The results in this paper suggest that targeting antioxidant enzymes with novel therapeutics may selectively kill off metastasizing cancer cells," Dr. Schafer said. The paper appears in the June 15, 2013 issue of Cancer Research, which is the most frequently cited cancer journal in the world. The research team collaborated with Dr. Matthew Leevy in Notre Dame's in vivo imaging facility.